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The exposome and pancreatic cancer, lifestyle and environmental risk factors for PDAC

G. Peduzzi, L. Archibugi, R. Farinella, RP. de Leon Pisani, L. Vodickova, P. Vodicka, B. Kraja, J. Sainz, D. Bars-Cortina, N. Daniel, R. Silvestri, P. Uysal-Onganer, S. Landi, J. Dulińska-Litewka, A. Comandatore, D. Campa, DJ. Hughes, C. Rizzato

. 2025 ; 113 (-) : 100-129. [pub] 20250512

Language English Country England, Great Britain

Document type Journal Article, Review

Persistent link   https://www.medvik.cz/link/bmc25015130

Pancreatic cancer (PC), particularly pancreatic ductal adenocarcinoma (PDAC), is a significant global health issue with high mortality rates. PDAC, though only 3 % of cancer diagnoses, causes 7 % of cancer deaths due to its severity and asymptomatic early stages. Risk factors include lifestyle choices, environmental exposures, and genetic predispositions. Conditions like new-onset type 2 diabetes and chronic pancreatitis also contribute significantly. Modifiable risk factors include smoking, alcohol consumption, non-alcoholic fatty pancreatic disease (NAFPD), and obesity. Smoking and heavy alcohol consumption increase PC risk, while NAFPD and obesity, particularly central adiposity, contribute through chronic inflammation and insulin resistance. Refined sugar and sugar-sweetened beverages (SSBs) are also linked to increased PC risk, especially among younger individuals. Hormonal treatments and medications like statins, aspirin, and metformin have mixed results on PC risk, with some showing protective effects. The gut microbiome influences PC through the gut-pancreas axis, with disruptions leading to inflammation and carcinogenesis. Exposure to toxic substances, including heavy metals and chemicals, is associated with increased PC risk. Glycome changes, such as abnormal glycosylation patterns, are significant in PDAC development and offer potential for early diagnosis. Interactions between environmental and genetic factors are crucial in PDAC susceptibility. Genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) linked to PDAC, but gene-environment interactions remain largely unexplored. Future research should focus on polygenic risk scores (PRS) and large-scale studies to better understand these interactions and their impact on PDAC risk.

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$a Pancreatic cancer (PC), particularly pancreatic ductal adenocarcinoma (PDAC), is a significant global health issue with high mortality rates. PDAC, though only 3 % of cancer diagnoses, causes 7 % of cancer deaths due to its severity and asymptomatic early stages. Risk factors include lifestyle choices, environmental exposures, and genetic predispositions. Conditions like new-onset type 2 diabetes and chronic pancreatitis also contribute significantly. Modifiable risk factors include smoking, alcohol consumption, non-alcoholic fatty pancreatic disease (NAFPD), and obesity. Smoking and heavy alcohol consumption increase PC risk, while NAFPD and obesity, particularly central adiposity, contribute through chronic inflammation and insulin resistance. Refined sugar and sugar-sweetened beverages (SSBs) are also linked to increased PC risk, especially among younger individuals. Hormonal treatments and medications like statins, aspirin, and metformin have mixed results on PC risk, with some showing protective effects. The gut microbiome influences PC through the gut-pancreas axis, with disruptions leading to inflammation and carcinogenesis. Exposure to toxic substances, including heavy metals and chemicals, is associated with increased PC risk. Glycome changes, such as abnormal glycosylation patterns, are significant in PDAC development and offer potential for early diagnosis. Interactions between environmental and genetic factors are crucial in PDAC susceptibility. Genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) linked to PDAC, but gene-environment interactions remain largely unexplored. Future research should focus on polygenic risk scores (PRS) and large-scale studies to better understand these interactions and their impact on PDAC risk.
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$a Archibugi, Livia $u Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Center, IRCCS Ospedale San Raffaele, Milan, Italy
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$a Farinella, Riccardo $u Department of Biology, University of Pisa, Pisa, Italy
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$a Vodickova, Ludmila $u Biomedical Center Martin, Bioinformatic Center, Comenius University in Bratislava, Jessenius Faculty of Medicine in Martin, Slovakia; Faculty of Medicine and Biomedical Center in Pilsen, Charles University, Pilsen, Czech Republic
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$a Vodicka, Pavel $u Biomedical Center Martin, Bioinformatic Center, Comenius University in Bratislava, Jessenius Faculty of Medicine in Martin, Slovakia; Faculty of Medicine and Biomedical Center in Pilsen, Charles University, Pilsen, Czech Republic
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$a Kraja, Bledar $u University Clinic of Gastrohepatology, University Hospital Center Mother Teresa, Tirana, Albania
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$a Sainz, Juan $u Department of Biochemistry and Molecular Biology, University of Granada, Granada, Spain; Centro de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBERESP), Madrid 28029, Spain; GENYO. Centre for Genomics and Oncological Research. Genomic Oncology department, Granada, Spain; Instituto de Investigación Biosanitaria Ibs.Granada, Granada, Spain
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$a Bars-Cortina, David $u Institut Català d'Oncologia (ICO) IDIBELL, Unit of Biomarkers and Susceptibility (UBS), Oncology Data Analytics Program (ODAP), Catalan Institute of Oncology (ICO), L'Hospitalet del Llobregat, Barcelona, Spain; Institut Català d'Oncologia (ICO) IDIBELL, ONCOBELL Program, Bellvitge Biomedical Research Institute (IDIBELL), L'Hospitalet de Llobregat, Barcelona, Spain
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$a Daniel, Neil $u Molecular Epidemiology of Cancer Group, UCD Conway Institute, School of Biomolecular and Biomedical Science, University College Dublin, Dublin, Ireland
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$a Silvestri, Roberto $u Department of Biology, University of Pisa, Pisa, Italy
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$a Uysal-Onganer, Pinar $u Cancer Mechanisms and Biomarkers Research Group, School of Life Sciences, University of Westminster, London, UK
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$a Landi, Stefano $u Department of Biology, University of Pisa, Pisa, Italy
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$a Dulińska-Litewka, Joanna $u Chair of Medical Biochemistry, Medical College, Jagiellonian University, Krakow, Poland
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$a Comandatore, Annalisa $u General Surgery Unit, Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Italy
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$a Campa, Daniele $u Department of Biology, University of Pisa, Pisa, Italy
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$a Hughes, David J $u Molecular Epidemiology of Cancer Group, UCD Conway Institute, School of Biomolecular and Biomedical Science, University College Dublin, Dublin, Ireland
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$a Rizzato, Cosmeri $u Department of Biology, University of Pisa, Pisa, Italy. Electronic address: cosmeri.rizzato@unipi.it
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